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Disentangling the manifold functions of RORγthttp://feeds.nature.com/~r/ni/rss/current/~3/citr_1n2BCI/ni.3831
A two-amino-acid substitution in the transcription factor RORγt disrupts its effect in establishing the transcriptional program of TH17 cells while leaving its function in the development of thymocytes and lymphoid-tissue–inducer cells largely intact.

A two-amino-acid substitution in the transcription factor RORγt disrupts its effect in establishing the transcriptional program of TH17 cells while leaving its function in the development of thymocytes and lymphoid-tissue–inducer cells largely intact.

]]>Disentangling the manifold functions of RORγtThomas Korndoi:10.1038/ni.3831Nature Immunology 18, 1059 (2017)2017-09-19Nature Immunology2017-09-1910.1038/ni.3831http://dx.doi.org/10.1038/ni.38311810News and Views10591060http://dx.doi.org/10.1038/ni.3831IFN-λ 'guts' neutrophil-mediated inflammationhttp://feeds.nature.com/~r/ni/rss/current/~3/rBhCEOM08MM/ni.3834
Interferon-λ (IFN-λ) curbs neutrophil-mediated intestinal inflammation by diminishing the production of reactive oxygen species and subsequent oxidative stress. This regulatory process is unique to IFN-λ and is independent of interferon-induced transcription and translation programs.

Interferon-λ (IFN-λ) curbs neutrophil-mediated intestinal inflammation by diminishing the production of reactive oxygen species and subsequent oxidative stress. This regulatory process is unique to IFN-λ and is independent of interferon-induced transcription and translation programs.

]]>IFN-λ 'guts' neutrophil-mediated inflammationEmily A HemannJohannes SchwerkRam Savandoi:10.1038/ni.3834Nature Immunology 18, 1061 (2017)2017-09-19Nature Immunology2017-09-1910.1038/ni.3834http://dx.doi.org/10.1038/ni.38341810News and Views10611062http://dx.doi.org/10.1038/ni.3834(T)Betting on innate lymphoid cells in CNS inflammatory diseasehttp://feeds.nature.com/~r/ni/rss/current/~3/YVoArVwSUvQ/ni.3839
T-bet+NKp46+ subsets of group 1 and group 3 innate lymphoid cells within the meninges initiate neuroinflammation in central nervous system (CNS)-demyelinating disease by regulating both the stability of pathogenic T-bet+ T cells and their access to the CNS.

T-bet+NKp46+ subsets of group 1 and group 3 innate lymphoid cells within the meninges initiate neuroinflammation in central nervous system (CNS)-demyelinating disease by regulating both the stability of pathogenic T-bet+ T cells and their access to the CNS.

]]>(T)Betting on innate lymphoid cells in CNS inflammatory diseaseMelissa A BrownAbigail E Russidoi:10.1038/ni.3839Nature Immunology 18, 1063 (2017)2017-09-19Nature Immunology2017-09-1910.1038/ni.3839http://dx.doi.org/10.1038/ni.38391810News and Views10631064http://dx.doi.org/10.1038/ni.3839B cell autoimmunity at the extremeshttp://feeds.nature.com/~r/ni/rss/current/~3/Y_GvNeR3KCw/ni.3840
Caveolin-1 has a critical role in orchestrating the membrane organization of B cells. In its absence, signaling via the B cell antigen receptor and B cell tolerance are impaired, which results in autoimmunity.

Caveolin-1 has a critical role in orchestrating the membrane organization of B cells. In its absence, signaling via the B cell antigen receptor and B cell tolerance are impaired, which results in autoimmunity.

]]>Ontogeny and function of murine epidermal Langerhans cellsDaniel H Kaplandoi:10.1038/ni.3815Nature Immunology 18, 1068 (2017)2017-09-19Nature Immunology2017-09-1910.1038/ni.3815http://dx.doi.org/10.1038/ni.38151810Review10681075http://dx.doi.org/10.1038/ni.3815The immunology of the allergy epidemic and the hygiene hypothesishttp://feeds.nature.com/~r/ni/rss/current/~3/6FTGxCMTfrM/ni.3829
Lambrecht and Hammad discuss how microbial diversity or dysbiosis influences epithelial barrier tissues and the impact of such interactions on the development of allergic disease.

]]>The immunology of the allergy epidemic and the hygiene hypothesisBart N LambrechtHamida Hammaddoi:10.1038/ni.3829Nature Immunology 18, 1076 (2017)2017-09-19Nature Immunology2017-09-1910.1038/ni.3829http://dx.doi.org/10.1038/ni.38291810Perspective10761083http://dx.doi.org/10.1038/ni.3829IFN-λ suppresses intestinal inflammation by non-translational regulation of neutrophil functionhttp://feeds.nature.com/~r/ni/rss/current/~3/4-H9tlZ00n4/ni.3821
The effect of the cytokine IFN-λ in non-epithelial cells remains unclear. Zanoni and colleagues show that IFN-λ specifically activates a signaling pathway that diminishes the production of reactive oxygen species and degranulation in neutrophils.

]]>IFN-λ suppresses intestinal inflammation by non-translational regulation of neutrophil functionAchille BroggiYunhao TanFrancesca GranucciIvan Zanonidoi:10.1038/ni.3821Nature Immunology 18, 1084 (2017)2017-08-28Nature Immunology2017-08-2810.1038/ni.3821http://dx.doi.org/10.1038/ni.38211810Article10841093http://dx.doi.org/10.1038/ni.3821The RNA helicase DDX46 inhibits innate immunity by entrapping m6A-demethylated antiviral transcripts in the nucleushttp://feeds.nature.com/~r/ni/rss/current/~3/77peHolGRpg/ni.3830
Helicases are vital to the induction of antiviral responses. Cao and colleagues demonstrate that the helicase DDX46 is involved in the epigenetic regulation of select RNA species encoding antiviral molecules, which leads to the retention of the RNAs in the nucleus and thus blockade of their translation and the activity of the proteins encoded.